Hearing IED 1

Pooja Bharamappa
Mind Map by Pooja Bharamappa, updated more than 1 year ago
Pooja Bharamappa
Created by Pooja Bharamappa over 6 years ago
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Description

Mind map based off lecture notes from Medsci 316 university of auckland

Resource summary

Hearing IED 1
  1. Oxidative Stress
    1. ROS

      Annotations:

      • FREE RADICALS - superoxide (02-) - hydroxyl radical (OH-) - peroxynitrite radical (ONOO-1-) GENERATE FREE RADICALS - h2o2 - ozone (O3)-
      1. CAUSE

        Annotations:

        • WHAT THEY CAUSE - common factor for hearing loss from noise, aminoglycoslide antibiotics, ototoxic anti cancer drugs, and raging
        1. ACTIONS

          Annotations:

          • WHAT THEY DO - ROS --> breakdown lipids and proteins in the membrane, damage DNA, 
          1. HOW FORMED

            Annotations:

            • HOW ARE THEY FORMED- noise --> electron transport chain of the mitochon uses a lot of O2 (lots of aerobic respiration) --> lots of SUPEROXIDE (unwanted by prod) is formed. superoxide goes and reacts with other stuff that generates more ROS
          2. Presbyacusis, Noise trauma, Ototoxic drugs COMMON FEATURES OF PATHOLOGY
            1. OHCS are affected and replaced by scars from supporting cells
              1. Spiral gang neurons degenerate
                1. Initial loss of basal cells and high frequencies
                2. Noise induced hearing loss
                  1. stereocilia damage

                    Annotations:

                    • highest impact is on stereocilia of the hair cells → mechanical damage → high amp movement of basilar memb, → stereocilia bent and distorted - prolonged exposure → cells will undergo apoptosis and die 
                    1. Glutamate excitotoxicity

                      Annotations:

                      • -->huge depol of cells and excessive release of Glutamate that acts on NMDA and AMPA receptors  --> swelling and destruction of post synp gang  --> this can recover, but prolonged exposure then  --> Ca entry to the synapse will eventually activate pro-apop pathways  --> loss of spiral gang neurons       
                      1. Inflammation

                        Annotations:

                        • there are many different inflame cells and these can cause damage to the delicate structure of the inner ear  --> diagram shows infiltration happening at spiral ligament
                        1. Apoptosis and Necrosis

                          Annotations:

                          • 1. apoptosis – process by which damaged cells are removed, diff cause, not well regulated, swelling of cells that will burst and spill their contents in ext cell space -> cause inflammation in the cochlea + organ of corti damaged in only one specific area --> many HCs are missing, many cells undergoing diff stages of apoptosis of necrosis 2. Necrosis – swelling of nuclei     
                          • 1. apoptosis – process by which damaged cells are removed, diff cause, not well regulated, swelling of cells that will burst and spill their contents in ext cell space -> cause inflammation in the cochlea + organ of corti damaged in only one specific area --> many HCs are missing, many cells undergoing diff stages of apoptosis of necrosis 2. Necrosis – swelling of nuclei     
                        2. AGE INDUCED HEARING LOSS
                          1. Epidemiology

                            Annotations:

                            • - Onset: 45 - 54 - 44% by 69 - 66% by 79  - >90% over age of 80
                            1. OVERVIEW

                              Annotations:

                              • - Env (trauma, aud stresses, otological diseases) + genetic factors (intrinsic, genetically controlled AGEING PROCESS) - loss begins at HIGHEST FREQs - social isolation, depression, loss of self- esteem  - reduced hearing sensitivity  - reduced speech understanding in NOISY ENVs  - slowed central processing or acoustic info  - impaired localisation.  SUMMARY - env+gene + red sensitivity + localisation + speech, slowed central processing + depression,social isolation. (6)
                              1. Pathology

                                Annotations:

                                • - damage to SV --> stria atrophy  - loss of OHCs  - loss of spiral gang neutrons - degenerative processes in central aud pathways 
                                1. Classification

                                  Annotations:

                                  • 1. sensory (Ohcs) --> ENV NOISE TOX 2. neural (neuronal cell loss) 3. metabolic (strial atrophy) --> HEREDITARY 3. mixed and indeterminate 
                                  1. mechanisms

                                    Annotations:

                                    • - reduction of vascularisation in the SV - oxidative stress (MITO damage APOP pathways)  - apoptosis  - collagen damage (fibrocytes 2 and 4 --> K+ cycling disruption and therefore EP) - accumulative noise exposure (accumulative OX STRESS)
                                  2. Cochlear Aging: Animal Studies
                                    1. whats been done

                                      Annotations:

                                      • - degene of SV - loss of Na/K therefore reduced K secretion  - decline in EP (cant have transduction) dead battery hypothesis 
                                      1. Animal examples

                                        Annotations:

                                        • C57BL/6 - early onset hearing loss- ARHL (ahl) locus of the chrom 10 - carrying specific mutation in cadherin 23 imp for encoding component for hair cell tip link  CBA/CaJ- late onset hearing loss- ahl - resistance geneFisher (344 albino rat)- sensory ARHLMongolian gerbil - strial ARHL 
                                        1. Changes in coch BVs

                                          Annotations:

                                          • at 3months gerbils have very dense network of capillaries and are WIDE as they grow older --> capillary network much less dense + narrower + loss of connections with each other --> loss of vasculature --> atrophy of network at 18 months 
                                        2. Ototoxicity

                                          Annotations:

                                          • cause  - aminoglycoside ABs - platinum based chemotherapeutic agents  Both - damage hair cells in basal turn of organ of corti  - spiral gan neurons  - lateral wall tissues (func deficits)
                                          1. AMINOGLYOSIDE OTO

                                            Annotations:

                                            • - used in treatment of tuberculosis (streptomycin, gentamicin) - serious gram -ve back infections (back endocarditis, UTIs, pneumonia) 
                                            1. APOPTOTIC CELL DEATH

                                              Annotations:

                                              • ROS two forms of apoptosis - extrinsic (death R mediated apop) - intrinsic (mitochon mediated cascade) DIS DA ONE (next page)
                                              • Intrinsic mitochon mediated apoptosis - induced by aminoglycosides in cochlea  --> activation of stress activated JNK (protein kinases) --> with increase intracellular Ca and release of cytochrome C from mito --> cyt C --> activation of camasses 8, 9, 3--> cell death pathway 
                                              1. CISPLATIN AND CARBOPLATIN

                                                Annotations:

                                                • - Platnium containing anti cancer drugs (testicular, ovarian, bladder, head and neck, lung) --> nephrotoxicity, neurotoxicity, ototoxicity.  go on next page
                                                • Cisplatin toxicity - high incidence of hearing loss (80%) - ototox: tinnitus and bilateral high freq sensorineural hearing loss - prod of ROS --> capase dep app pathways  - ototox can be ameliorated by protective agents targeting oxidative stress and and apoptosis
                                              2. Treament and management of hearing loss
                                                1. The 5 things

                                                  Annotations:

                                                  • - reduce glutamate excitotoxicity (NMDA inhib) - ensure good coach BF - suppression of inflammation  - antioxidants to restore normal balance with the free radicals - inhibit apop pathways to preserve hair cells
                                                  1. FREE RADS and ANTIOX BALANCE

                                                    Annotations:

                                                    • we can preserve hair cells by increasing antiox supplies.  - application of exogenous anti-ox molecules or systematically in the body  - endogenously by sound conditioning 
                                                    1. ANTIOXS

                                                      Annotations:

                                                      • molecules that scavenge molecules and convert them to less dangerous molecules.  - glutathione - vitamins A C E - Mg - catalase - superoxide dismutase - various peroxides 
                                                      1. HAIR CELL REGENE

                                                        Annotations:

                                                        • gene transfer tech stem cells replacement Atoh1/GFP+ cells show morphological and molecular correlates of interaction and synaptogenesis
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